Nocturnal Hypoxemia Research Articles

The Impact of Lung Function on Sleep Monitoring in Obstructive Sleep Apnea Associated with Obstructive Lung Diseases: Insights from a Clinical Study.

Background/Objectives: Obstructive sleep apnea (OSA) and obstructive lung diseases (OLD) are common and interdependent respiratory disorders, where one condition may contribute to the development and worsening of the other (OLDOSA syndrome). The term OLDOSA syndrome includes two different conditions: Overlap syndrome (OVS: OSA + chronic obstructive pulmonary disease, COPD) and Alternative Overlap syndrome (aOVS: OSA + Asthma). Data on the interactions between lung function and respiratory monitoring during sleep in OLDOSA patients are few and controversial. Our study aims to evaluate the impact of lung function impairment on sleep breathing disorders, paying attention to the lack of literature about comparisons between OVS, aOVS, and the impact of small airways disease (SAD) in these patients. Methods: In total, 101 patients with a diagnosis of OSA and asthma or COPD underwent pulmonary function tests (PFTs) and nocturnal home sleep cardiorespiratory monitoring (HSCM). Exclusion criteria: Obesity hypoventilation syndrome (OHS) and other non-respiratory sleep disorders. Results: Sleep time with oxygen saturation below 90% (T90) was negatively correlated with forced expiratory volume in the first second, % of predicted (%FEV1), forced vital capacity, % of predicted (%FVC), forced expiratory flow at 25-75% of the pulmonary volume, % of predicted (%FEF25-75), and, after multivariable linear regression analysis, %FEF25-75 remained an independent factor for T90 with a negative correlation in mild and moderate OSA. Obstructive apnea index (oAI) and FEV1/FVC were negatively correlated in mild and moderate OSA. OVS presented with more severe OSA (higher AHI, oAI, and T90) and SAD (lower FEF25-75) compared to aOVS. Conclusions: This study highlights a possible interdependence between OLD and OSA; obstruction of the large and small airways at PFTs contributes to the worsening of these patients' nocturnal hypoxemia and obstructive events of the upper airway during sleep. Furthermore, this study shows that patients with OVS should be carefully monitored, as they present worse data at HSCM and have greater small airways involvement compared to aOVS.

Brain-Derived Neurotrophic Factor in the Acute and Early Recovery Period of Ischemic Stroke: The Role of Nocturnal Hypoxemia

Brain-Derived Neurotrophic Factor in the Acute and Early Recovery Period of Ischemic Stroke: The Role of Nocturnal Hypoxemia

Hypoxemia during rapid eye movement sleep mediates memory impairment in older adults at risk for dementia via CA1 hippocampal volume loss

AbstractBackground and PurposeObstructive sleep apnea is associated with increased dementia risk. Nocturnal hypoxemia, which can be more severe during rapid eye movement (REM) sleep, may be a key mechanism. This study examines how REM hypoxemia affects memory and explores whether hippocampal vulnerability to hypoxemia mediates this effect in older adults at risk for dementia.MethodsOlder adults aged ≥50 years (N = 338) with subjective or mild cognitive impairment (i.e., objective impairment) underwent neuropsychological, mood, and medical assessment, magnetic resonance imaging scanning (n = 135), and overnight polysomnography. Verbal learning and memory were assessed with the Rey Auditory Verbal Learning Test. REM sleep hypoxemia was measured using the Oxygen Desaturation Index‐3% (REM‐ODI). Hippocampal subfield (CA1, CA3, subiculum, and dentate gyrus) volumes were derived from T1 and high‐resolution hippocampus T2 scans. We determined whether the relationship between REM‐ODI and learning and memory was mediated by hippocampal subfield volume. Analyses were repeated in non‐REM sleep to determine whether the effects were REM‐specific.ResultsAlthough there was not a direct effect of REM‐ODI on verbal learning (p > 0.05) or memory (p > 0.05), mediation analyses showed a significant indirect effect of high REM‐ODI on poorer verbal learning (β = −0.09, 95% confidence interval [CI] = −0.238 to −0.005) and memory (β = −0.100, 95% CI = −0.255 to −0.005), which was mediated by CA1 volume. These associations were absent in non‐REM sleep (p > 0.05).ConclusionsHypoxemia during REM sleep may impair memory in people at risk for dementia by reducing CA1 hippocampal volume. Research is needed to explore whether interventions targeting REM sleep hypoxemia are protective against memory decline.

Impact of sleep disturbance on longitudinal cognitive performance in patients with transient ischemic attack or mild stroke

IntroductionSleep disturbances including obstructive sleep apnea (OSA) and poor sleep quality are common after stroke, while its association with cognitive changes following transient ischemic attack (TIA) or mild stroke remains unclear. We aim to determine whether sleep duration, OSA parameters, or nocturnal hypoxemia is associated with a greater cognitive decline after stroke. MethodsWe prospectively followed-up patients with acute TIA/mild stroke [National Institute Health Stroke Scale (NIHSS) < 7] who underwent baseline sleep questionnaire [Pittsburgh Sleep Quality Index (PSQI)], and serial cognitive assessments [Montreal Cognitive Assessment (MoCA) 5-min, Stroop Test] at baseline and one-year. We also evaluated apnea-hypopnea index (AHI) and nocturnal hypoxemia by Home Sleep Apnea Test (HSAT) at one-year. Primary outcome was one-year change in MoCA 5-min score. ResultsOne hundred and five patients with TIA/mild stroke (mean age 63 years, 65 % male) were included. Baseline short sleep (< 6 hour/night) and AHI ≥ 20/hour at one-year were independently associated with a decline in the MoCA 5-min total score after covariates adjustment [short sleep: β = −2.36 95 % confidence interval (CI) (−4.13, −0.59), p = 0.009; AHI ≥ 20/hour: β = −1.79 (−3.26, −0.32), p = 0.017; remained significant after multiple comparisons correction]. A lower mean MinSpO2 was associated with a decline in executive function [Stroop interference index: β = 0.29 (0.04, 0.53), p = 0.021], but not with MoCA 5-min score at one-year. Moderation analysis indicated AHI ≥ 20/hour was associated with a pronounced decline in executive function only in men. ConclusionsShort sleep after stroke onset, AHI ≥ 20/hour and nocturnal hypoxemia at one-year contributed to an impaired cognitive trajectory at one-year following stroke in patients with TIA/mild stroke.

Images in sleep medicine sleep-disordered breathing in Wolfram's syndrome - A near-fatal event

Wolfram syndrome (WS) is a rare autosomal-recessive genetic disorder. The authors report a case of a patient with WS and undiagnosed/untreated obstructive sleep apnea (OSA) associated with prolonged periods of apnea and hypopnea and nocturnal hypoxemia, which may have predisposed him to the development of a near-fatal event during sleep. Addressing sleep-disordered breathing in patients with WS could improve their quality of life and potentially their longevity.

Associations between obstructive sleep apnea and sleep characteristics with chronic kidney disease in rural Pennsylvania

Study objectivesTo examine the association between moderate-severe obstructive sleep apnea (msOSA) and sleep characteristics with chronic kidney disease (CKD) in a population of rural and urban adults in Pennsylvania. MethodsA cross-sectional study of 23,643 adults who underwent polysomnography (PSG) at a rural healthcare system in Pennsylvania between 2009 and 2019. Serum creatinine was abstracted from electronic health records to calculate estimated glomerular filtration rate (eGFR). CKD was defined as an eGFR <60 mL/min/1.73 m2. msOSA was defined as an apnea-hypoxia index (AHI) ≥15 events/hour. Poisson regression was performed to estimate the prevalence ratio (PR) of CKD for various sleep measures while adjusting for age, sex, race, smoking (never, former, current), body mass index, diabetes, and hypertension at time of PSG. ResultsIn this clinically-referred sample comprised of over one-third (35 %) rural individuals, the prevalence of CKD and msOSA was 9.4 % and 32.1 %, respectively. Patients with CKD had more severe OSA based on AHI and intermittent hypoxia profile and presented worse sleep quality across all studied measures. Having OSA was associated with a 13 % higher prevalence of CKD (95%CI: 1.04, 1.22). In addition, for every 5 % increment in sleep efficiency, the prevalence of CKD was 3 % lower (PR = 0.97, 95%CI: 0.96, 0.98). Significant associations that were in the expected direction were observed across most sleep characteristics in adjusted models. ConclusionsModerate-severe OSA, nocturnal hypoxemia, and disruptions to normal sleep duration, continuity, and architecture are associated with increased CKD prevalence in Pennsylvania adults. Management of OSA and/or sleep disturbances may be an opportunity to improve CKD outcomes. The unique health disparities among vulnerable rural populations are deserving of future study.

Randomized crossover trial of a demand oxygen delivery system in nocturnal hypoxemia

The newly developed portable oxygen concentrator with an auto-demand oxygen delivery system (auto-DODS) automatically switches between 3 sensitivities according to the negative pressure gradient of inhalation and supplies oxygen only during inhalation. The aim of this study was to verify the effectiveness and safety of auto-demand devices compared with a continuous flow oxygen concentrator, during sleep, in a randomized crossover noninferiority trial. We alternatively used an auto-DODS or a continuous-flow oxygen concentrator, all night on separate days for HOT (Home Oxygen Therapy) patients with nocturnal hypoxemic symptoms. The primary endpoints were the mean value of oxygen saturation (SpO2) over the total sleep time. The secondary endpoints included the efficacy endpoints and the safety endpoints. Regarding the primary endpoint, the difference in SpO2 between the auto-DODS and continuous flow was 0.835%. Since the upper limit of this difference did not exceed 2.8, which was set as the noninferiority margin, it was shown that the auto-DODS did not reduce SpO2 by at least 2.8% on average compared to continuous flow. No equipment failure or exacerbation of disease was observed, confirming the safety of the auto-DODS during the night.

Nocturnal Hypoxemia Is Associated with Sarcopenia in Patients with Chronic Obstructive Pulmonary Disease.

Rationale: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide. Our previous studies have identified that nocturnal hypoxemia causes skeletal muscle loss (i.e., sarcopenia) in invitro models of COPD. Objectives: We aimed to extend our preclinical mechanistic findings by analyzing a large sleep registry to determine whether nocturnal hypoxemia is associated with sarcopenia in patients with COPD. Methods: Sleep studies from patients with COPD (n = 479) and control subjects without COPD (n = 275) were analyzed. Patients with obstructive sleep apnea, as defined by apnea-hypopnea index ⩾ 5, were excluded. Pectoralis muscle cross-sectional area (PMcsa) was quantified using computed tomography scans performed within 1 year of the sleep study. We defined sarcopenia as less than the lowest 20% residuals for PMcsa of control subjects, which was adjusted for age and body mass index (BMI) and stratified by sex. Youden's optimal cut-point criteria were used to predict sarcopenia based on mean oxygen saturation during sleep. Additional measures of nocturnal hypoxemia were analyzed. The pectoralis muscle index (PMI) was defined as PMcsa normalized to BMI. Results: On average, males with COPD had a 16.6% lower PMI than control males (1.41 ± 0.44 vs. 1.69 ± 0.56 cm2/BMI; P < 0.001), whereas females with COPD had a 9.4% lower PMI than control females (0.96 ± 0.27 vs. 1.06 ± 0.33 cm2/BMI; P < 0.001). Males with COPD with nocturnal hypoxemia had a 9.5% decrease in PMI versus COPD with normal O2 (1.33 ± 0.39 vs. 1.47 ± 0.46 cm2/BMI; P < 0.05) and a 23.6% decrease compared with control subjects (1.33 ± 0.39 vs. 1.74 ± 0.56 cm2/BMI; P < 0.001). Females with COPD with nocturnal hypoxemia had an 11.2% decrease versus COPD with normal O2 (0.87 ± 0.26 vs. 0.98 ± 0.28 cm2/BMI; P < 0.05) and a 17.9% decrease compared with control subjects (0.87 ± 0.26 vs. 1.06 ± 0.33 cm2/BMI; P < 0.001). These findings were largely replicated using multiple measures of nocturnal hypoxemia. Conclusions: We defined sarcopenia in the pectoralis muscle using residuals that take into account age, BMI, and sex. We found that patients with COPD have a lower PMI than patients without COPD and that nocturnal hypoxemia was associated with an additional decrease in the PMI of patients with COPD. Additional prospective analyses are needed to determine a protective threshold of oxygen saturation to prevent or reverse sarcopenia due to nocturnal hypoxemia in COPD.

Expanding TBCE-related phenotype-novel variant causing rigid spine, eosinophilia, neutropenia, and nocturnal hypoxemia.

We report three patients with the novel variant c.100 + 1G > A of the TBCE gene and describe the presented clinical phenotype in detail. We also systematically reviewed the literature for clinical similarities and dissimilarities among all known patients with pathogenic TBCE variants. The clinical phenotype observed in patients with pathogenic TBCE variants is broader than previously described. Homozygous carriers of the c.100 + 1G > A variant exhibit a markedly milder clinical course, with no deviations in the calcium-phosphate metabolism and central nervous system pathology in MRI studies. Additionally, two patients manifest highly specific symptoms such as a rigid spine, eosinophilia, neutropenia, and nocturnal hypoxemia. Furthermore, cryptorchidism was observed in male patients. The identification of the pathogenic c.100 + 1G > A variant has thus far been limited to patients of Central-Eastern European descent, suggesting a potential founder mutation in this population.

Gefapixant as a P2X3 receptor antagonist treatment for obstructive sleep apnea: a randomized controlled trial.

Obstructive sleep apnea (OSA) is a highly prevalent disorder with serious health consequences but limited therapeutic options. For a subset of those with OSA, a key underlying mechanism is hypersensitive chemoreflex control of breathing. There is no approved therapy that targets this endotypic trait. Here we determine whether the P2X3 receptor antagonist gefapixant, which is predicted to attenuate hypersensitive carotid chemoreflexes, reduces OSA severity in patients with chemoreflex-dependent OSA. In a randomized placebo-controlled cross-over study, 24 patients with moderate-to-severe OSA (aged 39-68 years, non-CPAP users) whose disorder was partially responsive to supplemental oxygen (chemoreflex-dependent OSA) were treated with gefapixant 180 mg (or placebo) administered as tablets taken orally before bedtime for 7 days and assessed via overnight polysomnography. The primary analysis examined whether gefapixant treatment resulted in a greater reduction in the apnea-hypopnea index (AHI) from baseline than placebo. Gefapixant did not lower the AHI significantly more than placebo; the estimated ratio of the AHI on gefapixant versus placebo was 0.92 [90% CI: 0.73, 1.17]. Notably, nocturnal hypoxemia was increased (ratio of total sleep time with SpO2 <90% on gefapixant versus placebo = 2.08 [90% CI: 1.53, 2.82]), consistent with reduced chemoreflex output. Commonly reported adverse events with gefapixant included ageusia, dysgeusia, oral hypoaesthesia, nausea, somnolence, and taste disorders. Gefapixant, while generally well tolerated, did not reduce OSA severity in patients with chemoreflex-dependent OSA. P2X3 receptor antagonism is unlikely to provide an avenue for therapeutic intervention in OSA. Registry: ClinicalTrials.gov; Name: Safety and Tolerability of Gefapixant (MK-7264) in Participants With Obstructive Sleep Apnea (MK-7264-039); URL: https://clinicaltrials.gov/study/NCT03882801; Identifier: NCT03882801.

Thoracic Society of Australia and New Zealand clinical practice guideline on adult home oxygen therapy.

This Thoracic Society of Australia and New Zealand Guideline on the provision of home oxygen therapy in adults updates a previous Guideline from 2015. The Guideline is based upon a systematic review and meta-analysis of literature to September 2022 and the strength of recommendations is based on GRADE methodology. Long-term oxygen therapy (LTOT) is recommended for its mortality benefit for patients with COPD and other chronic respiratory diseases who have consistent evidence of significant hypoxaemia at rest (PaO2 ≤ 55 mm Hg or PaO2 ≤59 mm Hg in the presence of hypoxaemic sequalae) while in a stable state. Evidence does not support the use of LTOT for patients with COPD who have moderate hypoxaemia or isolated nocturnal hypoxaemia. In the absence of hypoxaemia, there is no evidence that oxygen provides greater palliation of breathlessness than air. Evidence does not support the use of supplemental oxygen therapy during pulmonary rehabilitation in those with COPD and exertional desaturation but normal resting arterial blood gases. Both positive and negative effects of LTOT have been described, including on quality of life. Education about how and when to use oxygen therapy in order to maximize its benefits, including the use of different delivery devices, expectations and limitations of therapy and information about hazards and risks associated with its use are key when embarking upon this treatment.

Nocturnal hypoxemic burden and micro- and macrovascular disease in patients with type 2 diabetes

BackgroundMicro- and macrovascular diseases are common in patients with type 2 diabetes mellitus (T2D) and may be partly caused by nocturnal hypoxemia. The study aimed to characterize the composition of nocturnal hypoxemic burden and to assess its association with micro- and macrovascular disease in patients with T2D.MethodsThis cross-sectional analysis includes overnight oximetry from 1247 patients with T2D enrolled in the DIACORE (DIAbetes COhoRtE) study. Night-time spent below a peripheral oxygen saturation of 90% (T90) as well as T90 associated with non-specific drifts in oxygen saturation (T90non − specific), T90 associated with acute oxygen desaturation (T90desaturation) and desaturation depths were assessed. Binary logistic regression analyses adjusted for known risk factors (age, sex, smoking status, waist-hip ratio, duration of T2D, HbA1c, pulse pressure, low-density lipoprotein, use of statins, and use of renin-angiotensin-aldosterone system inhibitors) were used to assess the associations of such parameters of hypoxemic burden with chronic kidney disease (CKD) as a manifestation of microvascular disease and a composite of cardiovascular diseases (CVD) reflecting macrovascular disease.ResultsPatients with long T90 were significantly more often affected by CKD and CVD than patients with a lower hypoxemic burden (CKD 38% vs. 28%, p < 0.001; CVD 30% vs. 21%, p < 0.001). Continuous T90desaturation and desaturation depth were associated with CKD (adjusted OR 1.01 per unit, 95% CI [1.00; 1.01], p = 0.008 and OR 1.30, 95% CI [1.06; 1.61], p = 0.013, respectively) independently of other known risk factors for CKD. For CVD there was a thresholdeffect, and only severly and very severly increased T90non−specific was associated with CVD ([Q3;Q4] versus [Q1;Q2], adjusted OR 1.51, 95% CI [1.12; 2.05], p = 0.008) independently of other known risk factors for CVD.ConclusionWhile hypoxemic burden due to oxygen desaturations and the magnitude of desaturation depth were significantly associated with CKD, only severe hypoxemic burden due to non-specific drifts was associated with CVD. Specific types of hypoxemic burden may be related to micro- and macrovascular disease.

Management of sleep-disordered breathing in patients with syndromic hemifacial macrosomia.

Patients with syndromic hemifacial microsomia (SHFM) are at risk of obstructive sleep apnea (OSA). The aim of the study was to describe the prevalence of OSA and its management, especially in patients with Goldenhar syndrome (GS). The respiratory polygraphies and clinical management of 15 patients, aged 2 to 23years, evaluated at a national reference center, were analyzed. Four (27%) patients had no OSA, 4 (27%) had mild OSA, and 7 (46%), of whom 5 were ≤ 2years old, had severe OSA. None of the patients had central apneas. Only one patient had alveolar hypoventilation, and another one had nocturnal hypoxemia. Two patients had severe OSA despite prior adenoidectomy or mandibular distraction osteogenesis. Median duration of follow-up was 3.5years (range 0.5-9years). None of the patients without OSA or with mild OSA at baseline respiratory polygraphy developed OSA during the follow up. Among the 7 patients with severe OSA, 3 required continuous positive airway pressure or noninvasive ventilation, and one patient required a tracheostomy. In conclusion, patients with SHFM are at high risk of severe OSA at any age, underlining the importance of systematic sleep studies to diagnose and evaluate the severity of OSA. Individualized treatment should be privileged, based on a careful examination of the entire upper airway, taking in account potential associated risk factors. All patients with SHFM should be managed by a pediatric expert multidisciplinary medical/surgical team until the end of post pubertal growth.

Effects of acetazolamide on sleep disordered breathing in pulmonary vascular disease: a randomised controlled trial.

Patients with pulmonary vascular disease (PVD) often suffer from nocturnal hypoxaemia, but also from sleep apnoea. Short-term use of acetazolamide increases ventilation due to metabolic acidosis and also reduces loop gain. We investigated whether prolonged use of acetazolamide improves sleep disordered breathing in PVD. In a randomised controlled crossover trial, patients with PVD were randomly assigned to acetazolamide 250 mg and placebo twice daily for 5 weeks. Patients underwent respiratory polygraphy at baseline and at the end of each intervention phase. Outcomes of interest were the effect of acetazolamide on mean nocturnal oxygen saturation (S pO2 ), time with oxygen saturation <90% (t <90), apnoea-hypopnoea index (AHI) and sleep apnoea severity. In 20 patients with PVD (55% women, nine with pulmonary arterial hypertension, 11 with distal chronic thromboembolic pulmonary hypertension; mean±sd nocturnal S pO2 88.8±3.5%, obstructive AHI 12.6±12.3 events·h-1), 5 weeks of acetazolamide resulted in a significant improvement in nocturnal oxygenation compared to placebo (mean nocturnal S pO2 +2.3% (95% CI 1.3-3.3%); p<0.001 and t <90 -18.8% (95% CI -29.6- -8.0%); p=0.001). Acetazolamide increased the proportion of patients with mean nocturnal S pO2 ≥90% from 45% to 85%. The percentage of patients with AHI >5 events·h-1 was reduced from 75% to 60% and with AHI >15 events·h-1 from 30% to 15%. Two patients discontinued the study because of mild side-effects. Acetazolamide given for 5 weeks reduces nocturnal hypoxaemia in PVD to a clinically relevant level and reduces the proportion of patients with obstructive sleep apnoea.

Potential determinants of nocturnal hypoxemic burden and its association with atrial fibrillation recurrence after catheter ablation

Abstract Background Sleep-disordered breathing (SDB) is present in approximately half of patients with atrial fibrillation (AF) scheduled for catheter ablation (CA) and coincides with an elevated nocturnal hypoxemia. Purpose To evaluate determinants of nocturnal hypoxemic burden metrics and its association with AF recurrence after CA in patients undergoing a systematic SDB management and treatment pathway. Methods Consecutive AF patients scheduled for CA without history of SDB and/or SDB screening were included. Patients were referred to a virtual SDB management pathway including mobile health supported overnight home sleep test. An apnoea-hypopnoea index (AHI) of 5 to &amp;lt;15 and ≥ 15 were interpreted as mild and moderate-to-severe SDB, respectively. Oximetry data from home sleep tests were analyzed by a computer algorithm to evaluate metrics of nocturnal hypoxemic burden: time spent below 90% oxygen desaturation (T90) based on acute desaturations (T90 desat) or non-specific drifts in oxygen desaturation (T90 non-spec). Patients were monitored for AF recurrences through standard 12-lead ECG or Holter ECG and/or smartphone-based photophletysmography (PPG) performed at 3- and 12-month follow up. Multiple regression analysis was employed to (1) evaluate determinants of nocturnal hypoxemic burden metrics and (2) identify predictors of AF recurrence during 12 months after CA (excluding 3 months blanking period). Results The analysis included 210 patients (42% female, mean age 64± 9 years). Median AHI was 14.7 [6.7-24.7], median T90desat was 0.25 [0.03-1.42] minutes, T90non-spec 0.26 [0.08-0.78] minutes. Overall, 101 (48%) patients were diagnosed with moderate-to-severe SDB and 68 (32%) had mild SDB. Of patients with moderate-to- severe SDB and mild SDB, 87% and 46%, respectively, received a SDB therapy recommendation. Multiple linear regression analysis identified diabetes mellitus (B 8.611 95%CI 1.350-15.871, p=0.020) and AHI ≥ 15 (B 5.886, 95%CI 1.793-9.979, p= 0.005) as predictors of T90non-spec. Thyroid dysfunction (B 1.849, 95%CI 0.623-3.075, p=0.003) and AHI ≥ 15 (B 2.161, 95%CI 1.320-3.001, p&amp;lt;0.001) were significant predictors of T90desat. During 12 months after CA, 65 (31%) patients had experienced at least one AF recurrence after the blanking period. After multiple Cox-regression, age (HR 1.032, 95%CI 1.002-1.063, p= 0.035) and BMI ≥ 25 (HR 2.029, 95%CI 1.032-3.989, p=0.040) remained predictors for AF recurrences. Conclusions In AF patients scheduled for CA, SDB (AHI ≥ 15) and thyroid dysfunction were predictors for nocturnal hypoxemic burden with repetitive desaturations (T90desat). SDB and diabetes mellitus were predictors for nocturnal hypoxemic burden without repetitive desaturations (T90non-spec). In patients with AF who followed a virtual SDB management and treatment pathway, SDB presence and nocturnal hypoxemic burden metrics did not emerge as predictors, whereas age and BMI (≥25) remained significant predictors for AF recurrence.

Obstructive Sleep Apnea and Pulmonary Hypertension: A Chicken-and-Egg Relationship.

Obstructive sleep apnea (OSA) is characterized by repeated episodes of upper airway obstruction during sleep, and it is closely linked to several cardiovascular issues due to intermittent hypoxia, nocturnal hypoxemia, and disrupted sleep patterns. Pulmonary hypertension (PH), identified by elevated pulmonary arterial pressure, shares a complex interplay with OSA, contributing to cardiovascular complications and morbidity. The prevalence of OSA is alarmingly high, with studies indicating rates of 20-30% in males and 10-15% in females, escalating significantly with age and obesity. OSA's impact on cardiovascular health is profound, particularly in exacerbating conditions like systemic hypertension and heart failure. The pivotal role of hypoxemia increases intrathoracic pressure, inflammation, and autonomic nervous system dysregulation in this interplay, which all contribute to PH's pathogenesis. The prevalence of PH among OSA patients varies widely, with studies reporting rates from 15% to 80%, highlighting the variability in diagnostic criteria and methodologies. Conversely, OSA prevalence among PH patients also remains high, often exceeding 25%, stressing the need for careful screening and diagnosis. Treatment strategies like continuous positive airway pressure (CPAP) therapy show promise in mitigating PH progression in OSA patients. However, this review underscores the need for further research into long-term outcomes and the efficacy of these treatments. This review provides comprehensive insights into the epidemiology, pathophysiology, and treatment of the intricate interplay between OSA and PH, calling for integrated, personalized approaches in diagnosis and management. The future landscape of OSA and PH management hinges on continued research, technological advancements, and a holistic approach to improving patient outcomes.

Sleep-disordered breathing and nocturnal hypoxemia in chronic thromboembolic pulmonary disease.

Sleep-disordered breathing (SDB) and nocturnal hypoxemia were known to be present in patients with chronic thromboembolic pulmonary hypertension (CTEPH), but the difference betweenSDB and nocturnal hypoxemia in patients who have chronic thromboembolic pulmonary disease (CTEPD) with or without pulmonary hypertension (PH) at rest remains unknown. Patients who had CTEPH (n = 80) or CTEPD without PH (n= 40) and who had undergone sleep studies from July 2020 to October 2022 at Shanghai Pulmonary Hospital were enrolled. Nocturnal mean SpO2 (Mean SpO2) <90% was defined as nocturnal hypoxemia, and the percentage of time with a saturation below 90% (T90%) exceeding 10% was used to evaluate the severity of nocturnal hypoxemia. Logistic and linear regression analyses were performed to investigate the difference and potential predictor of SDB or nocturnal hypoxemia between CTEPH and CTEPD without PH. SDB was similarly prevalent in CTEPH and CTEPD without PH (P = 0.104), both characterised by obstructive sleep apnoea (OSA). Twenty-two patients with CTEPH were diagnosed with nocturnal hypoxemia, whereas only three were diagnosed with CTEPD without PH (P = 0.021). T90% was positively associated with mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance in patients with CTEPH and CTEPD without PH (P < 0.001); T90% was also negatively related to cardiac output in these patients. Single-breath carbon monoxide diffusing capacity, sex and mPAP were all correlated with nocturnal hypoxemia in CTEPH and CTEPD without PH (all P < 0.05). Nocturnal hypoxemia was worse in CTEPD with PH; T90%, but not SDB, was independently correlated with the hemodynamics in CTEPD with or without PH.

Obstructive Sleep Apnea and Nocturnal Hypoxemia Increase the Cardiovascular Risk in Chilean

To determine the association between the respiratory disturbance index (RDI) and the Time under 90% of SpO2 (CT90%) with CV risk using the predictive model of Framingham 2008. In addition, we analyzed the diagnostic performance of the baseline CV risk model, adjusted for RDI, CT90%, and their combination to predict CV mortality. in patients with clinical suspicion of AOS. Single-center prospective cohort study, including 1560 subjects. All patients underwent a clinical evaluation for OSA, blood pressure, and anthropometric variables. To determine the association of the indices of interest with CV risk, a linear multivariate regression was performed between the RDI or CT90% score. All analyses were performed using R software (R-project), and a p-value < 0.05 was considered statistically significant. RDI and CT90% showed significant differences for CV (p-value= <0.001). In addition, a percentage increase was demonstrated in each quartile of the RDI and CT90% (p-value= <0.001). The RDI and CT90% showed a significant and incremental association with the CV risk of the cohort. However, predictive analyses of CV mortality using the RDI and CT90% were not significant.

Influence of Impaired Diffusing Capacity and Sleep-disordered Breathing on Nocturnal Hypoxemia and Health Outcomes in Men with and without Human Immunodeficiency Virus.

Rationale: Nocturnal hypoxemia is common in sleep-disordered breathing (SDB) and is associated with increased morbidity and mortality. Although impaired diffusing capacity of the lung for carbon monoxide (DlCO) is associated with daytime hypoxemia, its influence on SDB-related nocturnal hypoxemia is not known. Objectives: To characterize the effects of DlCO impairment on SDB-related nocturnal hypoxemia and associated health outcomes. Methods: Data from a multicenter cohort of men with and without human immunodeficiency virus (HIV) infection, with concomitant measures of DlCO and home-based polysomnography (n = 544), were analyzed. Multivariable quantile regression models characterized associations between DlCO and several measures of SDB-related hypoxemia (e.g., total sleep time with oxygen saturation as measured by pulse oximetry [SpO2] < 90% [T90]). Structural equation models were used to assess associations of impaired DlCO and SDB-related hypoxemia measures with prevalent hypertension and type 2 diabetes. Results: DlCO impairment (<80% predicted) was associated with sleep-related hypoxemia. Participants with severe SDB (apnea-hypopnea index ⩾ 30 events/h) and impaired DlCO had higher T90 (median difference, 15.0% [95% confidence interval (CI), 10.3% to 19.7%]) and average SDB-related desaturation (median difference, 1.0 [95% CI, 0.5 to 1.5]) and lower nadir SpO2 (median difference, -8.2% [95% CI, -11.4% to -4.9%]) and average SpO2 during sleep (median difference, -1.1% [95% CI, -2.1% to -0.01%]) than those with severe SDB and preserved DlCO. Higher T90 was associated with higher adjusted odds of prevalent hypertension (odds ratio, 1.39 [95% CI, 1.14 to 1.70]) and type 2 diabetes (odds ratio, 1.25 [95% CI, 1.07 to 1.46]). Conclusions: DlCO impairment in severe SDB was associated with sleep-related hypoxemia, prevalent hypertension, and type 2 diabetes. Assessment of SDB should be considered in those with impaired DlCO to guide testing and risk stratification strategies.

The clinical and hemodynamic characteristics of pulmonary hypertension in patients with OSA-COPD overlap syndrome

BackgroundOur study aimed to assess the clinical and hemodynamic characteristics of pulmonary hypertension (PH) in patients with overlapping obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD), referred to OSA-COPD overlap syndrome (OS). MethodsWe enrolled a total of 116 patients with OS, COPD, or OSA who underwent right heart catheterization (RHC) due to suspected PH. We conducted a retrospective analysis of the clinical and hemodynamic characteristics of these patients. ResultsAmong the three groups (OS group, n = 26; COPD group, n = 36; OSA group, n = 54), the prevalence of PH was higher in the OS group (n = 17, 65.4%)compared to OSA group (n = 26,48.1%) and COPD group (n = 20,55.6 %). Among three groups with PH, the superior vena cava pressure (CVP) and right ventricular pressure (RAP) were higher in the OS group than in the OSA group (P < 0.05). Patients in the OS and COPD groups had higher pulmonary artery wedge pressure (PAWP) than in the OSA group (14.88 ± 4.79 mmHg, 13.45 ± 3.68 mmHg vs. 11.00 ± 3.51 mmHg, respectively, P < 0.05). OS patients with PH exhibited higher respiratory event index (REI), time spent with SpO2 <90%, oxygen desaturation index (ODI), minimal SpO2 (MinSpO2) and mean SpO2 (MSpO2) compared to OS patients without PH. After adjusting for potential covariates, we found that MinSpO2 (OR 0.937, 95 % CI 0.882–0.994, P = 0.032), MSpO2 (OR 0.805, 95% CI 0.682–0.949, P = 0.010), time spent with SpO2 <90% (OR 1.422, 95% CI 1.137–1.780, P = 0.002), and FEV1 % pred (OR 0.977, 95 % CI 0.962–0.993, P = 0.005) were related to the development of PH. ConclusionsPatients with OS showed higher prevalence of PH, along with higher PAWP, CVP and RAP. Worse nocturnal hypoxemia was found in OS patients with PH.